This picture reveals the pathophysiology:

https://preview.redd.it/dl3dhnydxr4a1.png?wid...bb17602030

Noureddin described it here:

Quote:

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30:07: Let me walk you through this cartoon, and I want you to look at these pink cells. What happens in these pink cells is that once you start getting like the fat deposition and injury , what that accumulation does, is cellular stress . And you see that arrow , and that leads to release of this chemokine CCL2 or MCP-1 . Once this is released, this is the bloodstream here on the top. What you see is these inflammatory cells, mainly circulating monocytes , start being recruited . And those are CCR2 , and this is very important. And these inflammatory monocytes, when they get to the liver, they raise a lot of chemokines and cytokines such as TNF alpha, IL-18, IL-6, Galactin, TGF-beta . And what that leads to is, you see these yellow cells, the stellate cells , those are the problems. If they get activated, they get to this, I guess, let's call it the monster activated myofibroblasts . Fibrous tissue becomes strong because of secreting collagen , and collagen is the mechanism of a scar .

31:29: Well, guess what? In these myofibroblasts , you see, you have the CCR5 receptor . So it's plausible that if you target CCR5, you stop a lot of this cascading, including inflammatory as well as the fibrosis signal . You're kind of at the right spot. And CCR5 is expressed in stellate cells and gets involved in the pro-fibrogenic activation proliferation pathway . So this is a key concept in the key area of the pathophysiology. TARGET CCR5

32:08: So what's CCR5? It's a G protein coupled receptors, and it's the receptor for these chemokines , where they hit and affect the cascade especially the harmful cascade . And its cognate ligands include CCL3, CCL4 and CCL5 (RANTES) . ( So Leronlimab also blocks CCL3, CCL4 as well as CCL5 ); And I showed you earlier that this important monocyte then that they turn into macrophages, and they activate the cascade inflammatory signal as well as eventually stellate cell itself to produce myofibroblast via CCR5 which is present on all these pathways, and CCR5 plays to this cascade mechanism.

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Our track record was flawed because we did not have proof that Leronlimab was safe and therefore we could not say it was effective either because, the only one in the room that can say it is safe is the FDA. When they lift the hold, the FDA will be saying it is safe. The peer reviewed article coming will say it is effective because the data will have been 4x validated against FDA GCP guidelines proving the drug is safe and then the data is worth per FDA to be analyzed.

With hold lifted, FDA is giving the go ahead to continue with further trials. The FDA trusts CytoDyn now to adhere to its rules when CytoDyn ventures in their game. FDA can trust Cyrus to play properly. The data is necessary. The prior trial CD NASH 01 was necessary to determine the dosages and determine what cytokines were affected. Leronlimab will deliver the unequivocal data in the coming trial, which will be what Cyrus needs to take this home.